RHINOVIRUS INHIBITS ANTIGEN-SPECIFIC T-CELL PROLIFERATION THROUGH AN INTERCELLULAR-ADHESION MOLECULE-1-DEPENDENT MECHANISM

To determine whether binding of human rhinovirus (HRV) to intracellula r adhesion molecule-1 might disrupt airway immune processes, effects o f a major HRV group, KRV-16, on T cell proliferation and cytotoxicity were defined. HRV (1-10 TCID50/cell) significantly inhibited T cell pr oliferation induced by antigen but not proliferation secondary to mito gens, interleukin-2, or an irradiated allogeneic T cell line. Noninfec tious (UV-irradiated) HRV had similar effects, Inhibition of T cell pr oliferation was dependent on HRV binding to intercellular adhesion mol ecule-1 on monocytes, indicating that the virus interferes with lympho cyte activation indirectly through effects on antigen-presenting cells . In addition, HRV inhibited T cell cytotoxic responses but not NK cel l activity, If these effects also occur in vivo, the resulting disturb ance in local airway immunity could increase the chances of successful viral replication, and might also be a factor in the pathogenesis of secondary viral or bacterial respiratory tract infections.